ReviewJournal of molecular and cellular cardiology2008
Mechanisms and potential therapeutic targets for ventricular arrhythmias associated with impaired cardiac calcium cycling.
Review in Journal of molecular and cellular cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Beat-to-beat QT interval variability as a tool to detect the underlying cellular mechanisms of arrhythmias.The Journal of physiology · 2025Article
- Loss of protein phosphatase 2A regulatory subunitFrontiers in cardiovascular medicine · 2024Article
- Automaticity in ventricular myocyte cell pairs with ephaptic and gap junction coupling.Chaos (Woodbury, N.Y.) · 2022Article
- Tracking nitroxyl-derived posttranslational modifications of phospholamban in cardiac myocytes.The Journal of general physiology · 2019Article
- The cardiac ryanodine receptor, but not sarcoplasmic reticulum CaThe Journal of biological chemistry · 2018Article
- SK channel enhancers attenuate Ca2+-dependent arrhythmia in hypertrophic hearts by regulating mito-ROS-dependent oxidation and activity of RyR.Cardiovascular research · 2017Article
- Effects of zacopride, a moderate IPharmacological research · 2017Article
- Suppression of ryanodine receptor function prolongs Ca2+ release refractoriness and promotes cardiac alternans in intact hearts.The Biochemical journal · 2016Article
- Phospholamban ablation rescues the enhanced propensity to arrhythmias of mice with CaMKII-constitutive phosphorylation of RyR2 at site S2814.The Journal of physiology · 2016Article
- Sarcoplasmic reticulum Ca²⁺ release is both necessary and sufficient for SK channel activation in ventricular myocytes.American journal of physiology. Heart and circulatory physiology · 2014Article
- Decreased RyR2 refractoriness determines myocardial synchronization of aberrant Ca2+ release in a genetic model of arrhythmia.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Store-dependent deactivation: cooling the chain-reaction of myocardial calcium signaling.Journal of molecular and cellular cardiology · 2013Review
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- Formation of spatially discordant alternans due to fluctuations and diffusion of calcium.PloS one · 2013Article
- Shortened Ca2+ signaling refractoriness underlies cellular arrhythmogenesis in a postinfarction model of sudden cardiac death.Circulation research · 2012Article
- Metabolic stress, reactive oxygen species, and arrhythmia.Journal of molecular and cellular cardiology · 2012Review
- Chronic CaMKII inhibition blunts the cardiac contractile response to exercise training.European journal of applied physiology · 2012Article
- The relationship between arrhythmogenesis and impaired contractility in heart failure: role of altered ryanodine receptor function.Cardiovascular research · 2011Article
- MicroRNA-1 and -133 increase arrhythmogenesis in heart failure by dissociating phosphatase activity from RyR2 complex.PloS one · 2011Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The close relationship between life-threatening ventricular arrhythmias and contractile dysfunction in the heart implicates intracellular calcium cycling as an important underlying mechanism of arrhythmogenesis. Despite this close association, however, the mechanisms of arrhythmogenesis attributable to impaired calcium cycling are not fully appreciated or understood. In this report we review some of the current thinking regarding arrhythmia mechanisms associated with either abnormal impulse initiation (i.e. arrhythmia triggers) or impulse propagation (i.e. arrhythmia substrates). In all cases, the mechanisms are primarily related to dysfunction of calcium regulatory proteins associated with the sarcomere. These findings highlight the broad scope of arrhythmias associated with abnormal calcium cycling, and provide a basis for a causal relationship between cardiac electrical instability and contractile dysfunction. Moreover, calcium cycling proteins may provide much needed targets for novel antiarrhythmic therapies.
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Registered trials
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